Dilated cardiomyopathy (DCM) is the most common cardiomyopathy associated with heart failure; however, the underlying mechanism remains unclear. Initially, gene expression data of patients with DCM from the GSE4172 and GSE21610 datasets were obtained from the Gene Expression Omnibus website. Differentially expressed genes (DEGs) were analyzed with a false discovery rate < 0.05 and log2 fold change > 1.2. Furthermore, both the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and Gene Set Enrichment Analysis (GSEA) were used to investigate the functional annotations. STRING and Cytoscape tools were used to form the protein-protein interaction (PPI) network and authenticate hub genes. Thereafter, the signature of immune-related genes (IRGs) was selected from the DEGs and data via the IMMPORT website. Hub genes were selected from the differentially expressed IRGs that formed the PPI network. Finally, the receiver-operating characteristic curves of the key genes were measured as biomarkers of DCM. A total of 173 independent DEGs (103 upregulated and 70 downregulated genes) were found in the microarray datasets GSE4172 and GSE21610. KEGG analysis and GSEA indicated that the BMP signaling pathway and apoptosis-related signals have a key effect on DCM development. The 10 hub genes also indicated the key effect of the BMP signaling pathway on DCM. A total of 224 differentially expressed IRGs and 20 featured IRGs were identified. Finally, BMP6, CD69, RUNX2, and SPP1 were identified as possible targets for DCM. Our data suggest a possible molecular regulatory mechanism for DCM therapy. Moreover, BMP6, CD69, RUNX2, and SPP1 may have key effects on the development of DCM.